Advanced glycation end-products induced VEGF production and inflammatory responses in human synoviocytes via RAGE-NF-κB pathway activation

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CCN4 induces IL-6 production through αvβ5 receptor, PI3K, Akt, and NF-κB singling pathway in human synovial fibroblasts

(2013) Chun-Han Hou et al.   ARTHRITIS RESEARCH & THERAPY

High glucose induces vascular endothelial growth factor production in human synovial fibroblasts through reactive oxygen species generation

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The role of synovitis in osteoarthritis pathogenesis

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Crosstalk between Advanced Glycation and Endoplasmic Reticulum Stress: Emerging Therapeutic Targeting for Metabolic Diseases

(2012) Christina Piperi et al.   JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM

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Advanced glycation end products cause collagen II reduction by activating Janus kinase/signal transducer and activator of transcription 3 pathway in porcine chondrocytes

(2011) C.-Y. Huang et al.   RHEUMATOLOGY

HMGB-1 induces IL-6 production in human synovial fibroblasts through c-Src, Akt and NF-κB pathways

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Advanced glycation end products induce the expression of interleukin-6 and interleukin-8 by receptor for advanced glycation end product-mediated activation of mitogen-activated protein kinases and nuclear factor- B in human osteoarthritis chondrocytes

(2010) Z. Rasheed et al.   RHEUMATOLOGY

Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis

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Sulfasalazine blocks the release of proteoglycan and collagen from cytokine stimulated cartilage and down-regulates metalloproteinases

(2009) R. L. Lakey et al.   RHEUMATOLOGY

Advanced glycation end products induce cell cycle arrest and proinflammatory changes in osteoarthritic fibroblast-like synovial cells

(2009) Sybille Franke et al.   ARTHRITIS RESEARCH & THERAPY

The NF- B Family of Transcription Factors and Its Regulation

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Current concepts in the pathogenesis of osteoarthritis

(2008) S. Krasnokutsky et al.   OSTEOARTHRITIS AND CARTILAGE

Effects of advanced glycation end products on the expression of COX-2, PGE2 and NO in human osteoarthritic chondrocytes

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